Exosomal miR-205-5p contributes to the immune liver injury induced by trichloroethylene: Pivotal role of RORα mediating M1 Kupffer cell polarization.

Trichloroethylene (TCE) is a common environmental contaminant that can induce occupational dermatitis medicamentosa-like TCE (ODMLT), where the liver damage is the most common complication. The study aims to uncover the underlying mechanism of TCE-sensitization-induced liver damage by targeting specific exosomal microRNAs (miRNAs). Among the enriched serum exosomal miRNAs of ODMLT patients, miR-205-5p had a significant correlation coefficient with the liver function damage indicators. Moreover, retinoic acid receptor-related orphan receptor α (RORα) was identified as a direct target of miR-205-5p via specific binding. Further experiments showed that kupffer cells (KCs) underwent M1 phenotypic and functional changes in liver injury induced by TCE which were alleviated by reducing the expression of miR-205-5p. However, this alleviation was reversed by the RORα antagonist SR1001. In vitro experiments showed that miR-205-5p promoted M1 polarization of macrophages and enhanced the secretion of inflammatory factors by regulating RORα. An increase in RORα reversed the polarization direction of M1-type macrophages and reduced the secretion of proinflammatory factors. In addition, pretreatment of mice with SR1078, a specific RORα agonist, effectively blocked M1 polarization of KCs and reduced the severity of TCE-induced liver injury. Our study uncovers that miR-205-5p regulates KC M1 polarization by targeting RORα in immune liver injury induced by TCE sensitization, providing new insight into the molecular mechanisms and new therapeutic targets for ODMLT.

Analysis of serum microRNAs and rs2910164 GC single-nucleotide polymorphism of miRNA-146a in COVID-19 patients.

Alteration of micro-RNAs (miRNAs) expression, including miRNA-122a, -146a and -205 family members, can have profound effects on inflammatory and IFN pathways (miRNA-146a), known as hallmarks of COVID-19. SARS-CoV-2-infected patients were recruited at Policlinico Umberto I Hospital of Sapienza University of Rome (Italy). MiRNA-122a, -146a, -205 and IFI27 (Interferon Alpha Inducible Protein 27) levels were screened in SARS-CoV-2 patients (n = 14) and healthy controls (n = 10) by real-time RT-PCR assays. Then, miRNA-146a rs2910164 GC single-nucleotide polymorphism (SNP) was genotyped in a larger group of COVID-19 patients (n = 129), and its relationship with severe disease [Intensive Care Unit (ICU) support or survival/death] was assessed. SARS-CoV-2-positive patients had increased PCR, D-Dimer and Fibrinogen levels compared to healthy controls (p < .05 for all measurements). MiRNA-122a and -146a serum levels were upregulated in COVID-19 patients (miRNA-122a: p = .002; miRNA-146a: p < .001). Decreased IFI27 levels were observed in COVID-19 patients with higher miRNA-146a levels (p = .047). Moreover, miRNA-146a rs2910164 C/G genotypes distributions were similar in COVID-19 patients and in validated European healthy subjects (n = 37,214). MiRNA-146a SNP was not associated with severe COVID-19 outcome (ICU or death). MiRNA-122a and -146a levels were elevated in SARS-CoV-2 infected patients, with miRNA-146a upregulation possibly contributing to IFN pathways dysregulation (e.g., reduced IFI27 levels) observed in severe COVID-19, although there is no evidence for the involvement of rs2910164 SNP.

Baicalin enhances the proliferation and invasion of trophoblasts and suppresses vascular endothelial damage by modulating long non-coding RNA NEAT1/miRNA-205-5p in hypertensive disorder complicating pregnancy.

AIM: Trophoblastic and vascular endothelial injuries were closely associated with the pathogenesis of hypertensive disorder complicating pregnancy (HDCP). The present study was designed to determine the functional role of baicalin in the proliferation and invasion of trophoblasts and vascular endothelial injury. METHODS: Ang II was adopted to stimulate HTR-8/SVneo and human umbilical vein endothelial cells (HUVECs). Cell viability was examined by CCK-8 assay. Flow cytometry and TUNEL staining determined cell apoptosis. Invasive ability of HTR-8/SVneo cells was measured by transwell assay. In vitro angiogenesis of HUVECs was assessed by Tube formation assay. In addition, the production of reactive oxygen species (ROS) was determined by DCFH-DA staining. Furthermore, long non-coding RNA (lncRNA) NEAT1 and miRNA-205-5p levels were detected using real-time quantitative polymerase chain reaction and the binding relationship between lncRNA NEAT1 and miRNA-205-5p was verified by dual-luciferase reporter assay. Moreover, interactions among lncRNA NEAT1, miRNA-205-5p, and MMP9 or vascular endothelial growth factor (VEGF) were confirmed by RNA immunoprecipitation assay. RESULTS: Baicalin visibly improved cell viability, reduced the apoptosis of Ang II-stimulated HTR-8/SVneo and HUVEC cells, and repressed overproduction of ROS. Additionally, baicalin promoted the invasion of Ang II-stimulated HTR-8/SVneo cells and induced a stronger in vitro angiogenesis of Ang II-stimulated HUVECs. What's more, baicalin upregulated lncRNA NEAT1 expression and downregulated miR-205-5p expression. LncRNA NEAT1 sponged miR-205-5p and inhibited the combination of miR-205-5p and MMP9 or VEGF. CONCLUSIONS: Baicalin can facilitate the proliferation and invasion of trophoblasts and alleviate vascular endothelial damage by upregulating lncRNA NEAT1 to impede the interaction between miR-205-5p and MMP9 or VEGF.

Resveratrol alleviates sepsis-induced acute kidney injury by deactivating the lncRNA MALAT1/MiR-205 axis.

INTRODUCTION: Resveratrol plays a protective role against sepsis development, and the long noncoding RNA (lncRNA) MALAT1 is an inflammation-relevant biomarker. This investigation attempted to reveal whether resveratrol attenuated inflammation of sepsis-induced acute kidney injury (AKI) by regulating MALAT1. MATERIAL AND METHODS: In total 120 rats were divided into a control group (n = 20), a Sham group (n = 20), a sepsis group (n = 40) and a resveratrol group (n = 40), and serum levels of inflammatory cytokines and AKI biomarkers were determined. An equal number of rats under identical treatments were, additionally, tracked for their survival, and the serum level of lncRNA MALAT1 was measured by RT-PCR. Moreover, septic cell models were constructed by treating HK-2 cells with lipopolysaccharide (LPS), and tumor necrosis factor α (TNF-α), interleukin (IL)-1ß, IL-6 levels released by the cells were determined with ELISA. RESULTS: Resveratrol treatment significantly brought down serum levels of inflammatory cytokines (i.e. TNF-α, IL-1ß and IL-6), kidney function indicators (i.e. Scr, blood urea nitrogen [BUN] and Scys C), AKI biomarkers (i.e. NGAL and KIM-1) and MALAT1 in cecal ligation and puncture (CLP)-induced septic model rats (all p < 0.05), and the life span of septic rats was elongated by resveratrol treatment (p < 0.05). Viability and cytokine release of LPS-treated HK2 cells were rescued by resveratrol (p < 0.05), which was accompanied by a marked fall of MALAT1 expression (p < 0.05). In addition, si-MALAT1 diminished viability and suppressed cytokine release of HK2 cells, while pcDNA3.1-MALAT1 hindered the impact of resveratrol on the inflammatory response of HK2 cells (p < 0.05). Ultimately, miR-205, a protective molecule in sepsis-relevant AKI, was down-regulated by resveratrol and si-MALAT1 (p < 0.05). CONCLUSIONS: Resveratrol relieved sepsis-induced AKI by restraining the lncRNA MALAT1/miR-205 axis.

Reawakening the master switches in triple-negative breast cancer: A strategic blueprint for confronting metastasis and chemoresistance via microRNA-200/205: A systematic review.

Triple-negative breast cancer (TNBC) exhibits a proclivity for early recurrence and development of metastasis. Moreover, drug resistance tends to arise few months following chemotherapeutic regimen with agents such as Doxorubicin, Paclitaxel, Docetaxel, and Cisplatin. miR-200 family and miR-205 are considered key regulators of metastasis by regulating the Epithelial-to-mesenchymal transition (EMT) via inhibiting ZEB1. Therefore, these microRNAs may offer therapeutic applications. Moreover, they hold potential for inhibiting chemoresistance and increasing chemosensitivity. These microRNAs are suppressed in TNBC cells. Increasing their levels, however, can inhibit EMT and improve progression-free survival (PFS). Besides using direct miRNA therapy via viral vectors, some drugs like Acetaminophen, or Tamoxifen are deemed useful for TNBC due to their ability to upregulate these miRNAs. In this review, by conducting an advanced search on PubMed, Embase, and Medline and selecting pertinent studies, we aimed to explore the potential applications of these microRNAs in controlling EMT and overcoming chemoresistance.

miRNA-205 affects infiltration and metastasis of breast cancer.

BACKGROUND: An increasing number of studies have shown that miRNAs are commonly deregulated in human malignancies, but little is known about the function of miRNA-205 (miR-205) in human breast cancer. The present study investigated the influence of miR-205 on breast cancer malignancy. METHODS: The expression level of miR-205 in the MCF7 breast cancer cell line was determined by quantitative (q)RT-PCR. We then analyzed the expression of miR-205 in breast cancer and paired non-tumor tissues. Finally, the roles of miR-205 in regulating tumor proliferation, apoptosis, migration, and target gene expression were studied by MTT assay, flow cytometry, qRT-PCR, Western blotting and luciferase assay. RESULTS: miR-205 was downregulated in breast cancer cells or tissues compared with normal breast cell lines or non-tumor tissues. Overexpression of miR-205 reduced the growth and colony-formation capacity of MCF7 cells by inducing apoptosis. Overexpression of miR-205 inhibited MCF7 cell migration and invasiveness. By bioinformation analysis, miR-205 was predicted to bind to the 3' untranslated regions of human epidermal growth factor receptor (HER)3 mRNA, and upregulation of miR-205 reduced HER3 protein expression. CONCLUSION: miR-205 is a tumor suppressor in human breast cancer by post-transcriptional inhibition of HER3 expression.

Expression of Long Noncoding RNA, HOTAIR, and MicroRNA-205 and Their Relation to Transforming Growth Factor ß1 in Patients with Alopecia Areata.

Introduction: Alopecia areata (AA) is a common autoimmune condition that affects anagen hair follicles. The most commonly recognized theory is that it is a T-cell-mediated autoimmune disorder in a genetically susceptible individual. MicroRNAs (miRNAs) and long noncoding RNAs (lncRNAs) were thought to play a function in the pathogenesis. The expression of lncRNA HOTAIR and miRNA-205 and their relation to transforming growth factor ß1 (TGF-ß1) in AA were not studied. Aim: The aim of the studywas to evaluate the role of miRNA-205, lncRNA, HOTAIR, and TGF-ß1 levels in AA pathogenesis, clinical course, and severity of AA. Methods: Two groups of subjects were included in this case-control study: 50 patients with AA and 50 healthy matched controls. miRNA-205 and lncRNA HOTAIR expression levels were assayed using quantitative RT-PCR, while serum levels of TGF-ß1 were assayed using ELISA techniques. Results: The serum expression of lncRNA HOTAIR was significantly downregulated in AA patients with a p value < 0.001, while the serum expression of both miRNA-205 and TGF-ß1 were significantly upregulated in patients. Discussion/Conclusion: This study highlights the potential role of high serum expression of miRNA-205 and TGF-ß1 and the low serum expression of lncRNA HOTAIR in AA pathogenesis. This could be used as a therapeutic target to treat AA.

A miRNA-205-based model for prediction of the recurrence of endometrioid endometrial cancer.

AIM: To develop a miRNA-205 based model for prediction of the recurrence of endometrial cancer. METHODS: The FIGO (International Federation of Gynecology and Obstetrics) stage, grading, myometrial infiltration, lymph node status and miRNA-205 expression levels were extracted from 90 endometrioid endometrial cancer patients, recurrence related risk factors were analyzed by Cox regression analysis. A risk model was then developed. RESULTS: A total of 90 endometrial cancer patients were retrospectively included for the analysis. The FIGO stage and expression levels of miRNA 205 were independently associated with the recurrence-free survival of the patients. The FIGO stage and expression levels of miRNA 205 were used for a prognostic model of recurrence-free survival. The c-index of the model reached 0.764, and the output of the model (risk score) could stratify the patients into different groups on the risk of recurrence. CONCLUSION: A miRNA-205 based model could predict the risk of recurrence for endometrioid endometrial cancer, and the model could provide a risk stratification of patients by recurrence risk.

ADSC-derived exosomes attenuate myocardial infarction injury by promoting miR-205-mediated cardiac angiogenesis.

BACKGROUND: Acute myocardial infarction is a major health problem and is the leading cause of death worldwide. Myocardial apoptosis induced by myocardial infarction injury is involved in the pathophysiology of heart failure. Therapeutic stem cell therapy has the potential to be an effective and favorable treatment for ischemic heart disease. Exosomes derived from stem cells have been shown to effectively repair MI injury-induced cardiomyocyte damage. However, the cardioprotective benefits of adipose tissue-derived mesenchymal stem cell (ADSC)-Exos remain unknown. This study aimed to investigate the protective effects of exosomes from ADSC on the hearts of MI-treated mice and to explore the underlying mechanisms. METHODS: Cellular and molecular mechanisms were investigated using cultured ADSCs. On C57BL/6J mice, we performed myocardial MI or sham operations and assessed cardiac function, fibrosis, and angiogenesis 4 weeks later. Mice were intramyocardially injected with ADSC-Exos or vehicle-treated ADSCs after 25 min following the MI operation. RESULTS: Echocardiographic experiments showed that ADSC-Exos could significantly improve left ventricular ejection fraction, whereas ADSC-Exos administration could significantly alleviate MI-induced cardiac fibrosis. Additionally, ADSC-Exos treatment has been shown to reduce cardiomyocyte apoptosis while increasing angiogenesis. Molecular experiments found that exosomes extracted from ADSCs can promote the proliferation and migration of microvascular endothelial cells, facilitate angiogenesis, and inhibit cardiomyocytes apoptosis through miRNA-205. We then transferred isolated exosomes from ADSCs into MI-induced mice and observed decreased cardiac fibrosis, increased angiogenesis, and improved cardiac function. We also observed increased apoptosis and decreased expression of hypoxia-inducible factor-1α and vascular endothelial growth factor in HMEC-1 transfected with a miRNA-205 inhibitor. CONCLUSION: In summary, these findings show that ADSC-Exos can alleviate cardiac injury and promote cardiac function recovery in MI-treated mice via the miRNA-205 signaling pathway. ADSC-Exos containing miRNA205 have a promising therapeutic potential in MI-induced cardiac injury.

Detection of plasma exosomal miRNA-205 as a biomarker for early diagnosis and an adjuvant indicator of ovarian cancer staging.

BACKGROUND: Ovarian cancer (OC) is one of the serious threats to the health of women worldwide, and accurate biomarkers are urgently demanded for early diagnosis of OC. We have previously confirmed that miR-205 promotes the invasion and metastasis of OC cells by inhibiting the expression of the tumor suppressor gene TCF21. In this study, we used liquid biopsy technology to detect the expression levels of the four genes, miR-205, CA125, HE4 and TCF21, in the exosomes of plasma of OC patients. Combined with analysis of clinicopathological parameters of OC patients, we aimed to provide efficient and non-invasive laboratory biomarkers for early diagnosis of OC. METHODS: 36 OC patients who were diagnosed in local hospitals from September 2020 to July 2021 were selected as OC group, 31 cases of surgically diagnosed with ovarian benign lesions were selected as benign group, and 32 healthy people who underwent physical examination during the same period were selected as a control group. We employed transmission electron microscope (TEM), Western blotting (WB), and nanoparticle tracking analysis (NTA) to identify biomarkers in the exosomes extracted from plasma of the three groups. The RNA levels of miR-205, CA125, HE4 and TCF21 genes in plasma exosomes were detected by real-time quantitative PCR (qRT-PCR) method. We used clinical pathological parameters and the Receiver Operating Characteristic (ROC) curves to evaluate the diagnostic efficacy for the genes detected in plasma exosomes. RESULTS: We found that the expression level of miR-205 in plasma exosomes of the OC group was significantly higher than that of the benign and control groups (P <  0.05), and the level of miR-205 was elevated during the III-IV periods of OC and lymph node metastasis. CONCLUSION: The level of miR-205 in plasma exosomes is a valuable tumor biomarker to improve OC diagnosis.

Etoposide-induced MicroRNA-205-5p Suppresses Proliferation and Migration by Targeting ERBB4 in MCF-7 Cells.

BACKGROUND/AIM: Patients with breast cancer frequently encounter a dismal prognosis due to the lack of effective and curative therapies. MicroRNAs (miRNAs) are aberrantly regulated in many types of cancer and have been recognized to play crucial roles in cancer progression. We performed a preclinical investigation of the anti-cancer effect of etoposide and microRNA-205-5p (miRNA-205-5p) and their relationship in MCF-7 cells. MATERIALS AND METHODS: Two cell culture systems, namely monolayers and spheroids, were employed for evaluating the effect of etoposide and miRNA-205-5p on cell proliferation and migration. Real time quantitative polymerase chain reaction was used for the measurement of mRNA and miRNA levels. Luciferase and western blot assays were utilized for the validation of the target gene of miRNA-205-5p. RESULTS: Treatment with etoposide, suppressed both cell proliferation and migration in MCF-7 monolayers. Also, the growth of MCF-7 spheroids as demonstrated by size measurements was inhibited by etoposide treatment. Furthermore, etoposide was found to upregulate the level of miRNA-205-5p. Over-expression of miRNA-205-5p inhibits cell proliferation and migration by directly targeting Erb-B2 receptor tyrosine kinase 4 (ERBB4). CONCLUSION: miRNA-205-5p may act as an important mediator of the anti-cancer effect of etoposide and miRNA-205-5p-based therapy may expand the therapeutic opportunities for breast cancer.

Exosomal miRNA-205 promotes breast cancer chemoresistance and tumorigenesis through E2F1.

Breast cancer (BC) is a common malignant tumor in females. The challenge in treating BC is overcoming chemoresistance. Exosome-mediated transfer of miRNAs is a molecule-shuttle in intercellular communication. Thus, we aimed to investigate whether exosomal miRNA-205 could affect chemoresistance and tumorigenesis in recipient tumor cells and to elucidate the underlying mechanism in vivo and in vitro. Microarray and qRT-PCR assays demonstrated that miRNA-205 was upregulated in tamoxifen resistance MCF-7/TAMR-1 (M/T) cells and M/T cell-derived exosomes (M/T-Exo). The M/T-Exo was internalized by human BC cells (BCCs), causing increased expression of miRNA-205 in BCCs. Coculturing with M/T-Exo promoted tamoxifen resistance, proliferation, migration, and invasion while suppressed apoptosis in recipient BCCs, which were associated with activating the caspase pathway and phosphorylating Akt. Luciferase reporter assays showed that miRNA-205 directly targeted E2F Transcription Factor 1 (E2F1) in BCCs. Furthermore, knockdown of miRNA-205 or overexpression of E2F1 reversed the roles of M/T-Exo in BCCs. In vivo experiments showed that the intratumoral injection of M/T-Exo caused greater tamoxifen resistance and larger tumor size relative to mice treated with miRNA-205-knockdown or E2F1-overexpressing BCCs. Together, the results suggest that exosomal miRNA-205 may promote tamoxifen resistance and tumorigenesis in BC through targeting E2F1 in vivo and in vitro.

The diagnostic value of miR-145 and miR-205 in patients with cervical cancer.

OBJECTIVE: To investigate the diagnostic value of miRNA-145 (miR-145) and miRNA-205 (miR-205) in cervical cancer patients. METHODS: Cervical tissue samples were collected from 144 patients diagnosed with and suspected to have cervical cancer in our hospital. Confirmed by pathology, 84 samples were obtained from cervical cancer patients and 60 samples were from patients with cervical intraepithelial neoplasia. Meanwhile, 30 patients with cervicitis were also selected, and the expression levels of miR-145, miR-205 and human papillomavirus (HPV) were detected in cervical lesions and normal cervical tissue. RESULTS: In comparison to normal cervical tissue, cervicitis and cervical intraepithelial neoplasia groups, the relative expression level of miR-145 was significantly lower, whereas the relative expression level of miR-205 was notably higher in the cervical cancer group, respectively (P<0.001). The area under the receiver operating characteristic (ROC) curve of miR-145 for diagnosis of cervical cancer in patients was 0.878, of which the sensitivity and the specificity were 0.905 and 0.822, respectively. The area under the ROC curve of miR-205 was 0.881, of which the sensitivity and the specificity was 0.869 and 0.889, respectively. Among all patients, the relative expression level of miR-145 was significantly lower while the relative expression level of miR-205 was considerably higher in HPV-positive patients than those of HPV-negative groups (P<0.001). Parauterine invasion, FIGO stage III-IV and lymphatic metastasis were considered as independent factors that affect the expression of miR-145. FIGO stage III-IV and lymphatic metastasis were independent factors affecting the expression of miR-205. CONCLUSION: The low expression level of miR-145 and the high expression level of miR-205 in patients with cervical cancer demonstrate a certain diagnostic value in cervical cancer. The expression level of miR-145 and miR-205 is correlated with HPV infection and cervical tumor malignancy.

The mediation of pigeon egg production by regulating the steroid hormone biosynthesis of pigeon ovarian granulosa cells.

The aim of this study was to determine the molecular mechanism of miR-205b targeting 11ß-hydroxysteroid dehydrogenase type 1 (HSD11B1) on the apoptosis and proliferation of granulosa cells (GC) of pigeons. Our previous studies suggested that HSD11B1 was the target gene of miR-205b and played a key role in steroid hormone biosynthesis and GC development. The adenovirus-miR-205b recombinant virus and adenovirus-cli-miR-205b-sh recombinant virus were generated, verified, and their characteristics determined. The recombinant viruses were used to infect the GC of pigeons, with real time quantitative PCR used to examine the expressions of HSD11B1 and related genes. The HSD11B1 antibody was obtained and verified, and Western blotting was used to detect the protein level of HSD11B1. The Cell Counting Kit-8 assay kit was used to detect cell viability, and the Annexin V-FITC/PI kit was used for the apoptosis assays. The expression of HSD11B1 was significantly lower in the overexpression (OE) than in OE negative control (OE-NC) treatments and significantly higher in short hairpin (SH) than in SH negative control (SH-NC) treatments. The expression levels of cytochrome P4503A5 was significantly higher in SH and lower in OE treatments, and the rhythms of cytochrome P450 aromatase mRNA levels were similar. The mRNA level of cytochrome P450scc in OE was lower than in OE-NC treatments and higher in SH than in SH-NC treatments. The protein expressions of HSD11B1 were decreased in the GC of OE, whereas increased in the SH group. The Cell Counting Kit-8 assay revealed that overexpression of miR-205b significantly suppressed proliferation of the GC of pigeons, whereas interference of miR-205b significantly induced the proliferation of the GC. The overexpression and the interference of miR-205b did not have a significant effect on cell cycle. The overexpression of miR-205b significantly increased the number of apoptotic cells, whereas the interference of miR-205b decreased the number of apoptotic cells. These findings indicated that miR-205b mediated pigeon egg production by regulating the steroid hormone biosynthesis of the pigeon ovarian GC by targeting HSD11B1, which may be useful in increasing pigeon egg production.

miR-205 targets angiogenesis and EMT concurrently in anaplastic thyroid carcinoma.

The current study aims to evaluate for the first time the inhibitory roles of miR-205 in the pathogenesis of anaplastic thyroid carcinoma. In addition, we investigated the mechanisms by which miR-205 regulates angiogenesis and epithelial-to-mesenchymal transition (EMT) in cancer. Two anaplastic thyroid carcinoma cell lines were transfected with the expression vector pCMV-MIR-205 Selected markers of angiogenesis and EMT including vascular endothelial growth factor A (VEGF-A) and zinc finger E-box-binding homeobox 1 (ZEB1) were investigated by Western blot. The interaction of miR-205 expression with EMT and angiogenesis were also investigated by assessment of matrix metalloproteinases 2 and 9 (MMP2 and MMP 9), SNAI1 (Snai1 family zinc finger 1), vimentin, E-cadherin and N-cadherin. The function of miR-205 was further tested with VEGF enzyme-linked immunosorbent assay (ELISA), wound healing, invasion and tube formation assays. Using an animal model, we studied the association of miR-205 with angiogenesis, proliferation and invasion. The following results were obtained. Permanent overexpression of miR-205 significantly suppressed angiogenesis and EMT by simultaneously targeting VEGF-A, ZEB1 and downstream products. Ectopic expression of miR-205 in cancer cells led to decreased migration, invasion and tube formation of endothelial cells. In addition, inhibition of tumour growth, vascularisation and invasion were noted in the mouse tumour xenografts. Our findings provide insights into simultaneous regulatory role of miR-205 in the pathogenesis of anaplastic thyroid carcinoma by suppressing both angiogenesis and EMT. This may open avenues to exploit miR-205 as an alternative cancer therapeutic strategy in the future.

MiR-205 promotes proliferation, migration and invasion of nasopharyngeal carcinoma cells by activation of AKT signalling.

OBJECTIVE: To examine the role of microRNA (miR)-205 in proliferation, migration and invasion of nasopharyngeal carcinoma (NPC). METHODS: The human NPC cell line CNE2 was transfected with miR-205 mimic, anti-miR-205 inhibitor or scrambled oligonucleotide (control). Cell proliferation was assessed via MTT assay. Cell migration and invasion were evaluated by transwell migration and Matrigel® invasion assay, respectively. Radiation induced apoptosis was quantified via Caspase-Glo3/7 assay. Apoptotic proteins and epithelial-mesenchymal transition (EMT) proteins were semiquantified by Western blot analysis. RESULTS: Overexpression of miR-205 increased the proliferation, migration and invasion of CNE2 cells, and decreased radiation-induced apoptosis compared with control cells. MiR-205 overexpression downregulated E-cadherin and upregulated Snail expression via downregulation of PTEN and upregulation of AKT. CONCLUSION: MiR-205 plays vital roles in tumourigenesis and tumour progression in NPC, and may be a potential treatment target.

The Role of MicroRNAs in the Regulation of K(+) Channels in Epithelial Tissue.

Our understanding of the modulation of proteins has shifted in direction with the discovery of microRNAs (miRs) over twenty years ago. MiRs are now in the "limelight" as these non-coding pieces of RNA (generally ~22 nucleotides long) result in altered translation and function of proteins. Indeed, miRs are now reported to be potential biomarkers of disease. Epithelial K(+) channels play many roles in electrolyte and fluid homeostasis of the human body and have been suggested to be therapeutic targets of disease. Interestingly, the role of miRs in modulating K(+) channels of epithelial tissues is only emerging now. This minireview focuses on recent novel findings into the role of miRs in the regulation of K(+) channels of epithelia.